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Pregnancy Induced Hypertension

Pregnancy Induced Hypertension. Jun Ma Dept. of Obstetrics & Gynecology The First Hospital of Xi’an Jiaotong Univ. Introduction. Incidence: China: 9.4%, worldwide: 7-12% The most common and yet serious conditions seen in obstetrics

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Pregnancy Induced Hypertension

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  1. Pregnancy Induced Hypertension Jun Ma Dept. of Obstetrics & Gynecology The First Hospital of Xi’an Jiaotong Univ

  2. Introduction • Incidence: China: 9.4%, worldwide: 7-12% • The most common and yet serious conditions seen in obstetrics • cause substantial morbidity and mortality in the mother and fetus • Death due to cerebral hemorrhage, aspiration pneumonia, hypoxic encephalophathy, thromboembolism, hepatic rupture, renal failure

  3. Hypertension in pregnancy Definition • Diastolic BP ≥90 mmHg • Systolic BP ≥140 mmHg • Or as an increase in the diastolic BP of ≥ 15 mmHg or in the systolic blood pressure of 30 mmHg, as compared to previous pressure • The increased blood pressures be present on at least two separate occasions, > 6h apart

  4. Classification

  5. Classification of Hypertensive Disorders in Pregnancy (ACOG) • Pregnancy-induced hypertension • Preeclampsia • Mild • Severe • Eclampsia • Chronic hypertension preceding pregnancy • Chronic hypertension with superimposed PIH • Superimposed preeclampsia • Superimposed eclampsia • Gestational hypertension

  6. Classification (1) • Pregnancy-induced hypertension: Hypertension associated with proteinuria and edema, occurring primarily in nulliparas after the 20th week or near term. Preeclampsia 【mild 】 • BP ≥ 140/90mmHg • Onset after 20 weeks’ gestation • Proteinuria (>300mg/24-hr urine collection) or + • Epigastric discomfort • Thrombocytopenia

  7. Classification (2) 【severe】 • BP ≥ 160/110 mmHg • Marked proteinuria (>1-2 g/24-hr urine collection or 2+ or more), oliguria • Cerabral or visual disturbances such as headache and scotomata • Pulmonary edema or cyanosis • Epigastric or right upper quadrant pain (probably caused by subcapsular hepatic hemorrhage) • Evidence of hepatic dysfunction, or thrombocytopenia

  8. Classification (3) Eclampsia • Meets the criteria of preeclampsia • Presence of convulsions, not attributable to other neurological disease, • Occurrence: 0.5 -4 %, with 25% occurring in the 1st 72 hs postpartum

  9. Classification (4) • Chronic hypertension proceeding pregnancy (essential or secondary to renal disease, endocrine disease, or other causes) • BP ≥ 140/90 mmHg • Presents before 20 wk gestation • Persists beyond 12 wk postpartum

  10. Classification (5) • Chronic hypertension with superimposed preeclampsia or eclamptia • Coexistence of preeclampsia or eclampsia with preexisting chronic hypertension • Cause greatest risk • When diagnosis is obscure, it is always wise to assume that the findings represent preeclampsia and treat accordingly.

  11. Classification (6) • Gestational hypertension: not mentioned in the ACOG • Finding of hypertension in late pregnancy in the absence of other findings suggestive or preeclampsia • Transient hypertension of pregnancy • May develop into chronic hypertension if elevated BP persists beyond 12 weeks postpartum

  12. High risk factors • Nulliparous • <18ys or >40 ys, multiple pregnancy • Has previous gestational hypertensive disorders • Chronic nephritis • Diabetic • Malnutrition • Low social status • Hydatidiform mole

  13. Etiology:UNCLEAR • Immune mechanism (rejection phenomenon, insufficient blocking Ab) • Injury of vascular endothelium----disruption of the equilibrium between vasoconstriction and vasodilatation, imbalance between PGI and TXA • Compromised placenta profusion • Genetic factor • Dietary factors: nutrition deficiency • Insulin resistance • Increase CNS irritability

  14. Pathophysiology

  15. Central nervous system • Raised BP disrupt autoregulation • Increased permeability due to vasospasm---thrombosis of arterioles, microinfarcts, and petechial hemorrhage • Cerebral edema: increased intracranial pressure • CT scan (1/3-1/2 positive): focal hypodensity • Cerebral angiography: diffuse arterial vasoconstriction • EEG: nonspecific abnormality (75% in eclamptic patient)

  16. Eyes • Serous retinal detachment • Cortical blindness

  17. Pulmonary system • Pulmonary edema • Cardiogenic or noncardiogenic • Excessive fluid retention, decreased hepatic synthesis of albumin, decreased plasma colloid oncotic pressure, • Often occurs postpartum • Aspiration of gastric contents: the most dreaded complications of eclamptic seizures

  18. Kidneys • Characteristic lesion of preeclampsia: glomeruloendotheliosis • Swelling of the glomerular capillary endothelium • Decreased GFR • Fibrin split products deposit on basement membrane • Proteinuria • Increase of plasma uric acid, creatinine,

  19. Liver • The spectrum of liver disease in preeclampsia is broad • Subclinical involvement • Rupture of the liver or hepatic infarction • HELLP syndrome: hemolysis, elevated liver enzymes and low platelets

  20. Cardiovascular system • Generalized vasoconstriction, low-output, high-resistance state • Untreated preeclamptic women are significantly volume-depleted • Capillary leak • Cardiac ischemia, hemorrhage, infarction, heart failure • Increased sensitivity to vasoconstrictor effects of angiotensin

  21. Blood (1) • Volume: reduced plasma volume • Normal physiologic volume expansion does not occur • Generalized vasoconstriction and capillary leak • Hematocrit

  22. Blood (2): coagulation • Isolated thrombocytopenia: <150,000/ml • Microangiopathic hemolytic anemia • DIC (5%) • HELLP syndrome: in severe preeclampsia • schistocytes on the peripheral blood smear • lactic dehydrogenase > 600 u/L • total bilirubin > 1.2 mg/dl • aspartate aminotransferase >70 U/L • platelet count <100,000/mm3 • Misdiagnosis: hepatitis, gallbladder disease, ITP

  23. Endocrine system • Vascular sensitivity to catecholamines and other endogenous vasopressors such as antidiuretic hormone and angiotensin II is increased in preeclampsia • Disequilibrium of prostacyclin/ thromboxane A2

  24. Placenta perfusion • 500 mm vs 200 mm • Acute atherosis of spiral arteries: fibrinoid necrosis of the arterial wall, the presence of lipid and lipophages and a mononuclear cell infiltrate around the damaged vessel----vessel obliteration---- placental infarction • Fetus is subjected to poor intervillous blood flow • IUGR or stillbirth

  25. Clinical findings (1) Symptoms and signs • Hypertension Diastolic pressure ≥ 90 mmHg or Systolic pressure ≥ 140 mmHg or Increase of 30/15 mmHg • Proteinuria • >300 mg/24-hr urine collection or • + or more on dipstick of a random urine

  26. Clinical findings (2) • Edema • Weight gain: 1-2 lb/wk or 5 lb/wk is considered worrisome • Degree of edema • Preeclampsia may occur in women with no edema • Most recent reports omit it from the definition

  27. Clinical findings (3) • Differing clinical picture in preeclampsia-eclampsia crises: patient may present with • Eclamptic seizures • Liver dysfunction and IUGR • Pulmonary edema • Abruptio placenta • Renal failure • Ascites and anasarca

  28. Clinical findings (4) Laboratory findings (1) Blood test: elevated Hb or Hct, in severe cases, anemia secondary to hemolysis, thrombocytopenia, FDP increase, decreased coagulation factors Urine analysis: proteinuria and hyaline cast, specific gravity > 1.020 Liver function: ALT and AST increase, alkaline phosphatase increase, LDH increase, serum albumin Renal function: uric acid: 6 mg/dl, serum creatinine may be elevated

  29. Clinical findings (5) Laboratory findings (2) Retinal check: Other tests: ECG, placenta function, fetal maturity, cerebral angiography, etc

  30. Differential diagnosis • Pregnancy complicated with chronic nephritis • Eclampsia should be distinguished from epilepsy, encephalitis, brain tumor, anomalies and rupture of cerebral vessel, hypoglycemia shock, diabetic hyperosmatic coma

  31. Complications • Preterm delivery • Fetal risks: acute and chronic uteroplacental insufficiency • Intrapartum fetal distress or stillbirth • IUGR • Oligohydramnios

  32. Predictive evaluation (1) • Mean arterial pressure, MAP= (sys. Bp + 2 x Dia. Bp) /3 • MAP> 85 mmHg: suggestive of eclampsia • MAP > 140 mmHg: high likelihood of seizure and maternal mortality and morbidity

  33. Predictive evaluation (2) • Roll over test: ROT • Preeclamptic patients are more sensitive to angiotensin II • Difference between Bp obtained at left recumbent position and supine position (at a 5 min interval) • Positive: > 20 mmHg • Urine calcium/ creatinine < 0.04

  34. Prevention • Calcium supplementation: not effective in low risk women bur show effect in high risk group • Aspirin (antithrombotic): uncertain • Good prenatal care and regular visits • Baseline test for high-risk women • Eclampsia cannot always be prevented, it may occur suddenly and without warning.

  35. Treatment • Mild preeclampsia: bed rest & delivery • Hospitalization or home regimen • Bed rest (position and why) and daily weighing • Daily urine dipstick measurements of proteinuria • Blood pressure monitoring • Fetal heart rate testing • Periodic 24-h urine collection • Ultrasound • Liver function, renal function, coagulation

  36. A. Mild preeclampsia: bed rest & delivery • Observe for danger signals: severe headache, epigastric pain, visual disturbances • Sedatives: debatable

  37. B. Severe preeclampsia: • Prevention of convulsion: magnesium sulfate or diazepam and phenytoin • Control of maternal blood pressure: antihypertensive therapy • Initiation of delivery: the definitive mode of therapy if severe preeclampsia develops at or > 36 wk or if there is evidence of fetal lung maturity or fetal jeopardy.

  38. Magnesium sulfate • Decreases the amount of acetylcholine released at the neuromuscular junction • Blocks calcium entry into neurons • Vasodilates the smaller-diameter intracranial vessels

  39. Magnesium sulfate • Prevent convulsion • Virtually ineffective on blood pressure • i.v. or i.m. • 5g loading dose 5-10 min, i.v. • 1-2g/hr constant infusion • Total dose: 20-30 g/d

  40. Toxicity: • Diminished or loss of patellar reflex • Diminished respiration • Muscle paralysis • Blurred speech • Cardiac arrest

  41. How to prevent toxicity? • Frequent evaluation of patellar reflex and respirations • Maintenance of urine output at >25 ml/hr or 600 ml/d • Reversal of toxicity: • Slow i.v . 10% calcium gloconate • Oxygen supplementation • Cardiorespiratory support

  42. Antihypertensive therapy:reduce the Dia. pressure to 90-110 mmHg Indication • Bp> 160/110 mmHg • Dia. Bp > 110 mmHg • MAP > 140 mmHg • Chronic hypertension with previous antihypertensive drugs usage

  43. Antihypertensive therapy Medications: • Hydrolazine: initial choice • Labetolol • Nifedipine • Nimoldipine • Methyldoe • Sodium nitroprusside

  44. Mechanism of action Effects Medication Direct peripheral vasodilation CO, RBF maternal flushing, headache, tachycardia hydralazine CO, RBF maternal flushing, headache, neonatal depressed respirations a, b- adrenergic blocker labetalol CO, RBF maternal orthostatic hypotension Headache, no neonatal effects Calcium channel blocker nifedipine Direct peripheral arteriolar vasodilation CO, RBF maternal flushing, headache, tachycardia methyldopa Metabolite (cyanide) toxic to fetus sodium nitroprusside Direct peripheral vasodilation

  45. Plasma expander • Diuretics

  46. Delivery • Indication of termination of pregnancy • Preeclampsia close to term • <34 wk with decreased placental function • 2 hs after control of seizure

  47. Delivery • Induction of labor • First stage: close monitor, rest and sedation • Second stage: shorten as much as possible • Third stage: postpartum hemorrhage • Cesarean section • Induction of labor unsuccessful • Induction of labor not possible • Maternal or fetal status is worsening

  48. Eclampsia • No aura preceding seizure • Multiple tonic-clonic seizures • Unconsciousness • Hyperventilation after seizure • Tongue biting, broken bones, head trauma and aspiration, pulmonary edema and retinal detachment

  49. Management • Control of seizure • Control of hypertension • Delivery • Proper nursing care

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